Wednesday, April 20, 2016

A 37 year old female with no comorbidities, a non-smoker, with no known hyperlipidemia and no family h/o of CAD presented to ED with central chest pain since 5 hours with no radiation, increased by moving her arms and associated with SOB. This occurred after a stressful interpersonal conflict. She had had similar episodes before when angry or stressed.

"I looked at the ECG and immediately thought "This is an acute LAD occlusion." It is diagnostic of LAD occlusion, but really only to someone who has expertise. You will virtually never see an EKG like this that is a patient's baseline. The T-waves are huge in proportion to the QRS, the QRS amplitude is very small, the T-waves are symmetric and fat, there are sagging ST segments in I, II, V3 and V4. V3 should have some ST elevation, but it actaully has a bit of ST depression."

She was discharged with diclofenac 75 mg IM injection. The pain was relieved.

The patient was discharged home with reassurance and analgesia.

12 hours later the patient was found collapsed at home with no signs of life. The family refused a post-mortem. As she visited our ED within 24 hours from her death, her ECG was reviewed and 50% of the consultants said there is no abnormality of in it. The other 50% said there are hyperacute T waves suggestive of early presentation of MI.

My response:

Sorry to hear about the outcome. This is a very hard ECG for a non-expert to recognize. My hope is that this blog, with cases like this, will educate others about these kinds of subtle findings and prevent future cases like this.

Other comment:

It would have been very helpful to record an ECG after the pain was relieved, to see if there is resolution of the hyperacute T-waves. I would not use absence of change to be reassured that this is NOT ischemia, as it is too abnormal to be anything else. But resolution (change) would be confirmatory evidence.

Learning Points:

1. We all must learn these high risk findings of coronary occlusion.

2. Hyperacute T-waves have a unique morphology. The are like a face that you must recognize.

3. Negative troponins must not be trusted in the setting of an ischemic ECG.I received a good question:So as we move to "rapid rule outs" do you think a second troponin would likely have shown a change? I am trying to understand if this is an acute problem how similar previous episodes are connected vs red herring.My answer:Not necessarily. Even with high sensitivity troponins, there will be false negatives. Not all unstable angina will be detected in the future by hs trop. You will still need to be able to read the ECG. For this patient:1) the artery could spontaneously open up before there is any cell death (i.e., before any elevation of troponin). Then, later, the lesion could close off and kill. Alternatively2) if the artery does not reperfuse, then by the time you have a second troponin back, most of the damage is done.You must be able to recognized these patterns or you will miss an opportunity to make a big difference.

Steve SmithSome more comments and answers that I want to feature:

Comment: Unfortunately without the post-mortem, or more information (which may not have been included in the article for brevity's sake), I would argue it is not possible to say for certain that an MI was missed here. Perhaps the cause of death was overdose, drugs, or some other factor. The fact that the family refused a post-mortem in this situation makes me think something else may have been at play.

Answer: But the EKG is diagnostic of LAD occlusion. That is by far the most likely cause of death.

Comment: T waves are not hyperacute by definition, and it's a difficult scenario. Looking retrospectively it's easy to say an echo would have been helpful but I would have probably done the same except repeating an ecg and two sets of troponins

Answer: They are indeed hyperacute. There is no definition. You just have to learn to recognize it. Denying it will just put you in trouble some day, and that's why I'm trying to teach you. I did not look retrospectively. I saw the ECG before I knew any outcome and knew immediately that it was LAD occlusion. Many of my readers tell me this was obvious, not even subtle. Rather than fighting it, try to learn this morphology. It may save a patient of yours. Learn. Don't be closed-minded.

THANKS to Dr. Stephen Smith for posting this highly illustrative case. There recently has been a good number of similar tracings like this posted on various ECG forums (each with slight variation from the other) — but ALL with virtually the SAME finding — namely that the T waves in lead V2 (and to a lesser extent in lead V3) are disproportionately tall compared to the amplitude of the QRS complex in these leads. And, the responses I’ve seen from even experienced clinicians show the same remarkable range as that reported by Dr. Smith in this Blog — namely that some clinicians correctly recognize the tracing for a DeWinter variant with acute occlusion (or about to be acute occlusion) of the proximal LAD — and others (unfortunately all-too-many other clinicians) call such findings “normal”.

THIS is a tracing that probably should be shown to ALL clinicians (MD and non-MD) who are called upon to analyze acute 12-lead ECGs — both for teaching and perhaps assessment of ECG interpretation ability … In my opinion, this is a case that just should NOT be missed because: i) the patient presented to an ED with 5 hours of chest pain — which should of itself dramatically lower your threshold for what is “normal” vs “abnormal”; ii) the T wave in lead V2 is almost twice QRS amplitude in this lead — and the width of this T wave is comparable to QRS amplitude in this V2 lead. There is no way this is normal in a patient wth new chest pain.

The findings in multiple other leads that Dr. Smith describes are more subtle, but given the picture described by i) and ii), they all support the diagnosis of DeWinter-like T waves.

Dependence on troponins (even the highest of sensitivity troponins) has no place in a case like this. I would be happy initial troponin was negative — since it means that we have recognized this acute LAD occlusion in time to dramatically improve prognosis.

Most cases of anterior hyperacute T waves will not be as glaring as this one is. But attention to the learning points of this case can markedly help to reduce the chance of oversight: i) When a patient presents to the ED with new chest pain — one has to look that much more carefully at their ECG; ii) Engrain the picture of the ST-T wave that we see in lead V3 in your mind. The ST-T wave in V3 is not as obvious as that in V2, but the T wave is still clearly disproportionately taller, fatter at its peak and wider at its base than it should be given QRS amplitude in this lead (Even without V2, this ECG should be of great concern; with V2 this ECG should be alarming); iii) Train your eye to look extra carefully at the “other leads” on the tracing for “patterns”. Virtually every lead on this tracing (except perhaps aVL) has at least a subtle abnormality that taken together in context with the history of new chest pain + obvious abnormality in V2,V3 adds further support of acuity until proven otherwise.

So as we move to "rapid rule outs" do you think a second troponin would likely have shown a change? I am trying to understand if this is an acute problem how similar previous episodes are connected vs red herring.

Not necessarily. Even with high sensitivity troponins, there will be false negatives. Not all unstable angina will be detected by hs trop. You will still need to be able to read the ECG. For this patient, the artery could spontaneously open up before there is any cell death (i.e., before any elevation of troponin). Then later, the lesion could close off and kill. Alternatively, if the artery does not reperfuse, then by the time you have a second troponin back, most of the damage is done.

You must be able to recognized these patterns or you will miss an opportunity to make a big difference.

Unfortunately without the post-mortem, or more information (which may not have been included in the article for brevity's sake), I would argue it is not possible to say for certain that an MI was missed here. Perhaps the cause of death was overdose, drugs, or some other factor. The fact that the family refused a post-mortem in this situation makes me think something else may have been at play.

T waves are not hyperacute by definition, and it's a difficult scenario. Looking retrospectively it's easy to say an echo would have been helpful but I would have probably done the same except repeating an ecg and two sets of troponins

Shahrukh,They are indeed hyperacute. There is no definition. You just have to learn to recognize it. Denying it will just put you in trouble some day, and that's why I'm trying to teach you. I did not look retrospectively. I saw the ECG before I knew any outcome and knew immediately that it was LAD occlusion. Many of my readers tell me this was obvious, not even subtle. Rather than fighting it, try to learn this morphology. It may save a patient of yours. Learn. Don't be closed-minded.Steve Smith

Thanks Dr Smith... Really appreciate the points you and Mr Ken Grauer have highlighted. Indeed for students like me, in our residency career, it is of paramount importance to look each and every Ecg in general and every leads in particular precisely and like in this case, could be life saving. I've always learnt néw points from your blog. Thanks again

I for one of the readers can say it is obvious to me. It is frankly one of the more obvious examples of hyperacute Ts that I have seen on this blog. Not because I'm better than others at reading ECGs, but because I think it is obvious to readers with an open mind who have read more than two of the many many posts almost exactly like this.

onset of symptoms 5 hours ago and no troponin? i guess it was not a hs-troponin - otherwise it should have been positive if that was really lad-occlusion. and if it was no hs-troponin, a second troponin should have been measured, even if the ecg was completely normal. anyhow...very interesting case! thanks for that!

Alex,you must understand the dynamic nature of ACS. Chest pain can be present for 5 hours without any infarction. Or pain can come and go for hours without any infarction. Also, in de Winter's paper, the de Winter's T-waves were persistent over long periods of LAD occlusion.I think this patient had intermittent occlusion.You cannot rely exclusively on troponin, even hs troponin. Unstable angine still exists and is deadly.Unfortunately, we still need physicians.Steve Smith

Thank you for your great cases. May I make a suggestion? The way I, and many others, work through your cases is to first attempt to read the ECG myself and then correlate with your interpretation. I usually open the ECG picture file in a new tab to be able to zoom in and really get a good look. However, the name of the file usually contains the diagnosis and is prominently displayed in the header. If it wasn't to much of a bother to your workflow it would be helpful if the title was less revealing. Just a suggestion. Either way your cases and this blog is amazing. Thank you again.

THANKS to Dr. Stephen Smith for posting this highly illustrative case. There recently has been a good number of similar tracings like this posted on various ECG forums (each with slight variation from the other) — but ALL with virtually the SAME finding — namely that the T waves in lead V2 (and to a lesser extent in lead V3) are disproportionately tall compared to the amplitude of the QRS complex in these leads. And, the responses I’ve seen from even experienced clinicians show the same remarkable range as that reported by Dr. Smith in this Blog — namely that some clinicians correctly recognize the tracing for a DeWinter variant with acute occlusion (or about to be acute occlusion) of the proximal LAD — and others (unfortunately all-too-many other clinicians) call such findings “normal”.

THIS is a tracing that probably should be shown to ALL clinicians (MD and non-MD) who are called upon to analyze acute 12-lead ECGs — both for teaching and perhaps assessment of ECG interpretation ability … In my opinion, this is a case that just should NOT be missed because: i) the patient presented to an ED with 5 hours of chest pain — which should of itself dramatically lower your threshold for what is “normal” vs “abnormal”; ii) the T wave in lead V2 is almost twice QRS amplitude in this lead — and the width of this T wave is comparable to QRS amplitude in this V2 lead. There is no way this is normal in a patient wth new chest pain.

The findings in multiple other leads that Dr. Smith describes are more subtle, but given the picture described by i) and ii), they all support the diagnosis of DeWinter-like T waves.

Dependence on troponins (even the highest of sensitivity troponins) has no place in a case like this. I would be happy initial troponin was negative — since it means that we have recognized this acute LAD occlusion in time to dramatically improve prognosis.

Most cases of anterior hyperacute T waves will not be as glaring as this one is. But attention to the learning points of this case can markedly help to reduce the chance of oversight: i) When a patient presents to the ED with new chest pain — one has to look that much more carefully at their ECG; ii) Engrain the picture of the ST-T wave that we see in lead V3 in your mind. The ST-T wave in V3 is not as obvious as that in V2, but the T wave is still clearly disproportionately taller, fatter at its peak and wider at its base than it should be given QRS amplitude in this lead (Even without V2, this ECG should be of great concern; with V2 this ECG should be alarming); iii) Train your eye to look extra carefully at the “other leads” on the tracing for “patterns”. Virtually every lead on this tracing (except perhaps aVL) has at least a subtle abnormality that taken together in context with the history of new chest pain + obvious abnormality in V2,V3 adds further support of acuity until proven otherwise.

I would think repeat ecgs are absolutely necessary for any patient with chest pain. We tend to undermine the risk of MI in adult women.

I would repeat ecg every 15-30 min, until I am satisfied (although I agree that the initial ecg is an LAD lesion staring at my face) if the patient is asymptomatic I would be hesitant to call the cath lab and this is where I think I ll repeat ecgs frequently and monitor in a chest pain unit.

This case highlights few important aspects 1. MI occurs more frequently than we think in adult females.2.recognition of critical lesions which can be subtle.3. Repeat ecgs and am not sure if rapid rule out hs cTn can help here.

Same problem here Dr.Smith, we don't have a cath lab and while my attendings understand that this is a LAD problem, they are not willing to thrombolyse, not only De Winter's but also Wellen's, which are considered STEMI equivalents. They prefer to send the patient to another shop 2hours away from ours. How do you think that i can persuade them to use lytics in such cases? Is there any literature convincing enough(for them not me..i am just the resident)? Thank you very much

Can you get an immediate high quality echo? Prove to them with wall motion abnormality. Also, Wellens' is NOT a STEMI equivalent! Wellens' is a syndrome when the patient has had pain, is not pain free, and the artery is open. The T-wave inversions are due to reperfusion of an artery that was occluded at the time of the pain, but spontaneously opened. There is non-occlusive thrombus and TIMI 3 flow. Do not give lytics. Emergent PCI is not necessarily indicated, but aggressive antiplatelet, antithrombotic, therapy is, plus continuous 12-lead ECG to monitor for re-occlusion.Steve Smith

Very interesting but also very sad case! Thanks! We also had a young man in his 20's with no cardiac risk factors, no drugs etc. who had a sudden onset of central chest pain with hyperacute t waves in multiple leads. ECG then switched to normal. A week later we had dramatic t wave inversion in just the leads where those very tall t waves were seen. So we guessed unstable angina. Cardiac enzymes turned out normal. Coronary angiogram was done - normal. Nevertheless patient died a few weeks later at home. What it was? - no idea. Do you guys have a guess/idea?

Angiogram can miss such ischemia due to:1) spasm2) non-stenotic atheroslerosis with complete lysis of thrombus. Only intravascular ultrasound can find these disrupted plaques.In 5-10% of ACS, the coronary angiogram (which is a lumen-o-gram, and does not detect extravascular plaque) does not show a culprit!Steve

Troponins (conventional or highly sensitive) are really only designed to rule out in low risk cases. Despite this pt being apparently low risk due to minimal risk factors, her ECG is ischaemic which would mean being unable to use a risk stratification tool such as the Heart pathway. Troponin usage does not excuse you from engaging brain and evaluating the patient in front of you. This patient had an MI and it was missed.

Another diagnostic consideration in this case is Takotsubo cardiomyopathy. This fits with the patient's age, sex, lack of risk factors for CAD and can also cause sudden death. The ECG changes while suggestive of LAD occlusion, are not 100% specific for this condition and the pre-test probability is low. T wave changes such as this would be atypical for Takotsubo but have been reported. Serial ECGs, repeat troponin and urgent echo would have clarified the diagnosis.

See above. Her age makes it just as unlikely to be Takotsubo as LAD occlusion. Takotsubo is much more common in elderly.

See this study: http://www.ahjonline.com/article/S0002-8703(12)00240-2/abstract

BackgroundThe aim of this study was to describe the prevalence of Takotsubo cardiomyopathy (TTC), age-gender interaction, and various comorbidities associated with it based on nationwide hospitalization records. Takotsubo cardiomyopathy is an increasingly reported clinical syndrome; however, there are no data on its prevalence in the general US population.

MethodsThe Nationwide Inpatient Sample discharge records were queried for the year 2008 using the International Classification of Diseases, Ninth Revision, code 429.83.

ResultsThere were 6,837 patients diagnosed with TTC among 33,506,402 hospitalizations in the Nationwide Inpatient Sample database. Women were found to have higher odds of developing TTC (odds ratio 8.8). Women >55 years old had 4.8 times higher odds for developing TTC when compared with women <55 years old. Smoking, alcohol abuse, anxiety states, and hyperlipidemia were commonly associated with TTC. The peak incidence of hospitalization for TTC was in summer.

ConclusionTakotsubo cardiomyopathy was diagnosed in about 0.02% of all hospitalizations in the United States, mostly in elderly women with history of smoking, alcohol abuse, anxiety states, and hyperlipidemia.

Thank you for this postingFor pt with chest pain, yes the morphology of t wave and amplitude are consider as alarming sign,What I like to stress onSerial ECG would help,specially, after the pain has subsided,

Thank you for posting this caseThe morphology and the amplitude of t wave are alarming sign in this case , the fact that ,the patient came with chest pain,Serial ECG would help specially after the chest pain has been subsided to compare .Thank you dr smith

Why would such a high T not taken into account? I believe the "rule" to be T<R/2, isn't it? moreover, would you not think at the very least of a possible ion disturbance?I'm just starting with ECG so my knowledge may be not proper at all, correction or comments would be highly appreciated!

Doctor...Thank you. As a CC-paramedic I would have definitely noted, and reported, the "abnormal" T waves, but frankly, would not have known just what they meant. When I see these in patients in the field my intent is to take them directly to a cardiac center (ours is typically in St. Paul), and advocate for a closer look at the patient than MIGHT otherwise occur. I sometimes get my wrist slapped (not often) for over advocating, but I don't mind.

I immediately recognized the ECG pattern of this instructive case since I have learned de Winter’s T waves time ago thanks to your highly appreciated teaching in this blog. Thank you, Dr. Smith!On the other hand I am still perplexing regarding the paucity of interest neither in literature nor even in guidelines on this STEMI-equivalent. For those interested, let me point out the latest paper on the topic by the way by the author of this ECG pattern (de Winter, Adams, Verouden, de Winter J Electrocardiol 2016 Jan-Feb; 49(1):76-80---it is mainly a cases report but it provides also a brief review on the topic and the admission by the author himself that the de Winter’s pattern could not be solely persistent). Mario

This is a tragic case. If there was ever one that highlighted why we must learn ECG patterns it's this one. This ECG screams LAD OCCLUSION, but only for those that know what to look for. Our eyes will never see ECG patterns that our minds do not know. Learning these patterns is what ECG reading is all about. As EPs, we must master this domain of Emergency Medicine. In my opinion it is as important as airway, or any other aspect of our job. I do not know anyone who has made as big an impact in this regard as you have. Thanks for all that you have done and that you continue to do.

This would be a difficult case at my shop. I agree with the diagnosis/ the hyperacute t-waves in relation to the QRS are the most concerning, I don't know what to make of the sagging st segments except that it is subtle dewinters morphology. Our cath lab activation is more like an interventional stat consult, they get the ekg and we speak to them, and they decide whether to cath or not. I can tell you this case would be rejected, I've had patient's with <1mm elevation in contiguous leads and a good story get rejected because they don't meet classic criteria, and they end up making troponins and relabeled as an NSTEMI. In light of a rejected cath lab activation, I probably would get serial ecgs (more than just one repeat) and admitted the patient, to telemetry if they accepted her.

I wonder if there's anything we can do in the ED to support our case for cath lab activation with a bullish interventional group, you think if I asked the patient to jog a lap around the ER and repeated the ecg if that would help?

Get a high quality contrast echocardiogram to prove wall motion abnormality. Get q 1 hour troponins, if necessary. But do NOT just admit to telemetry. That will prevent sudden death (by detecting V Fib), but it will result in loss of the anterior wall.

I am a junior serving primary health care, if a patient like yours, aka. no risk factors, presented to us with chest pain and this was the ECG, it would be very difficult to convince the tertiary hospital that she was having LAD occlusion. With our hospitals and cardiac centers being overcrowded, how do I stand firm that this could be an MI or impending MI?Thank you

Yes, wonderful case. As noted previously, please rename the image files on these cases before you upload them. Please use a name other than the actual diagnosis, so that the downloaded file name doesn't tell me the answer before I can even study the EKG! Above all, please keep up the great interactive teaching, answering questions so that all of us can do the best for our patients.

R wave progression was poor in V leads and the ST's were, indeed, elevated. Septal MI? II, III, AVF indicate, to me, an inferior, as well.Sad case. And another woman dies because she did not "fit" the standard . Alarming SOB and pain in arms were ignored.

Hi,I am very surprised that in the ER doctors didn't try nitroglycerine in this patient. This occlusion is probably a coronary spasm and even if this test could be misleading in case of oesophageal spasm it would have been useful to confirm a link between EKG and clinical setting.

This is much more likely to be coronary thrombosis. Thrombi propagate and lyse constantly, proven by intravascular angiooscopy. Spasm is only diagnosed when there is a negative angiogram, and even then requires intravascular ultrasound, as angiograms are only lumenograms which often fail to diagnose the ruptured plaque after the lysis of the thrombus.

Thank you for this excellent case. I must agree that this ECG has acute LAD occlusion written all over it. Beside the ST depression and hyperacute T waves the one thing that is extremely concerning is that I struggled to find 1 normal lead without ischaemic changes. I am a cardiology fellow working in a South African academic hospital. I am finding more and more often in our emergency rooms and even with our internal medicine trainees that doctors are over reliant on troponin blood results to make they diagnosis of acute coronary syndromes. It is resulting on patients like this being sent home who have concerning ECG changes and typical pain but negative troponins. My advice to them is usually that it is not a sin to ask for a second opinion and to escalate the case. Troponins are an excellent test but what I have noticed also is when a negative troponin is received and the ECG like the one above is missed and a repeat trop is requested that it results in hours of delay in revascularizing a patient. Its basically like saying I want to wait for muscle to start dying before I react to it. And the golden hour is lost which greatly worsens a patient's prognosis. Furthermore if one is seeing a patient with chest pain it is thought that the pain is "non-cardiac" then a diagnosis should be sought as there are numerous other life-threatening causes of chest pain which should be ruled out .. such as an aortic aneurism or pulmonary embolism. Thank you for the case. Its sad for the patient but the lesson is to learn to recognise these infarct patterns so that they aren't missed in the future.Regards.

GREAT comments Bradley! Yet every day new sponsored studies on the "benefits of troponins" seem to come out, whereas in reality simple history, targeted brief physical exam, careful ECG assessment, and sometimes bedside Echo are really all one needs for optimal clinical decision-making in the vast majority of cases. To depend too much on the troponin I think often means suboptimal attention to the other factors.

The converse is true also in that a mildly positive troponin doesn't necessarily mean acute coronary syndrome either. Recently Professor Jean Marco from France visited our department and highlighted this point very well in showing a case with positive troponins which was sent to the cardiology team who took the patient to the cath lab.. they found some disease but nothing critical. Then the patient went into shock and was taken back to cath lab as their ACS case with positive trops must have some disease which the doctor had originall missed. The patient demised on the table. At post-mortem: A saddle embolism which presented with positive trops. I really think it is a good test and very useful. But the evaluation of possible coronary artery disease doesn't begin and end with the trops. Its merely one aspect. The clinical picture, history, clinical exam, ECG, echo is where the money is at. I usually use the troponins more of a prognostic test to show how much muscle has died between onset of pain and revascularization.

@ Bradley Brits — I am just curious — Was there "telltale" anterior T wave inversion on ECG of that patient you describe above who was taken to cath because of "positive troponin", and then died on the tble of a saddle embolus ... ? One of the most common oversights/misinterpretations is to equate anterior T wave inversion = coronary disease/ischemia — when at times this may be a classical picture of acute Right-Heart "Strain".

It was exactly what was on the ECG. I think in general a good history, clinical exam, ECG evaluation and probably bedside echo combined should be sufficient to make a good assessment in almost all cases. Thinking back to the case of the pulmonary embolism: a good echo was lacking in the patients assessment. Finding the accompanying regional wall motion abnormality correlating with the ECG findings is gold.

Thanks for sharing this. I found it a useful and thought-provoking reminder even though I am not in EM or primary care. Am very glad to have found your blog and look forward to reading your other posts.

Thanks for the excellent case! It must not be overlooked that this patient was a young woman. Would this tracing have been as easily overlooked in a 70 yo man? I don't think so. Physicians must improve treatment of women in both ED and clinic settings. Although less common in some populations heart disease knows no age or gender. Not only MI but ischemia from coronary spasm including widespread microvascular spasm is easily missed when clinicians assume stress or panic first without scrutinizing the ecg. Cases of ischemia from spasm are plagued by equivocal ischemic ecg changes and negative initial troponins. Women are often pushed out the door before before the levels can rise or a repeat ecg can clarify the situation. We must do a better job when women, especially young women, come in complaining of chest pain.

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Cases come from all over the world. Patient identifiers have been redacted or patient consent has been obtained. The contents of this site have not been reviewed nor approved by Hennepin County Medical Center and any views or opinions expressed herein do not necessarily reflect the views or opinions of Hennepin County Medical Center.